Ganong's Review of Medical Physiology, 23rd Edition

160
SECTION II
Physiology of Nerve & Muscle Cells

CENTRAL CONNECTIONS

OF AFFERENT FIBERS

Ia fibers end directly on motor neurons supplying the extrafus-
al fibers of the same muscle (Figure 9–3). The time between the
application of the stimulus and the response is called the
reac-
tion time.
In humans, the reaction time for a stretch reflex
such as the knee jerk is 19–24 ms. Weak stimulation of the sen-
sory nerve from the muscle, known to stimulate only Ia fibers,
causes a contractile response with a similar latency. Because the
conduction velocities of the afferent and efferent fiber types are
known and the distance from the muscle to the spinal cord can
be measured, it is possible to calculate how much of the reac-
tion time was taken up by conduction to and from the spinal
cord. When this value is subtracted from the reaction time, the
remainder, called the
central delay,
is the time taken for the re-
flex activity to traverse the spinal cord. In humans, the central
delay for the knee jerk is 0.6–0.9 ms, and figures of similar mag-
nitude have been found in experimental animals. Because the
minimal synaptic delay is 0.5 ms, only one synapse could have
been traversed.
Muscle spindles also make connections that cause muscle
contraction via polysynaptic pathways, and the afferents
involved are probably those from the secondary endings.
However, group II fibers also make monosynaptic connec-
tions to the motor neurons and make a small contribution to
the stretch reflex.

FUNCTION OF MUSCLE SPINDLES

When the muscle spindle is stretched, its sensory endings are

distorted and receptor potentials are generated. These in turn

set up action potentials in the sensory fibers at a frequency pro-

portional to the degree of stretching. Because the spindle is in

parallel with the extrafusal fibers, when the muscle is passively

stretched, the spindles are also stretched, referred to as “loading

the spindle.” This initiates reflex contraction of the extrafusal fi-

bers in the muscle. On the other hand, the spindle afferents

characteristically stop firing when the muscle is made to con-

tract by electrical stimulation of the

α

-motor neurons to the ex-

trafusal fibers because the muscle shortens while the spindle is

unloaded (Figure 9–4).

Thus, the spindle and its reflex connections constitute a

feedback device that operates to maintain muscle length; if

the muscle is stretched, spindle discharge increases and reflex

shortening is produced, whereas if the muscle is shortened

without a change in

γ

-motor neuron discharge, spindle affer-

ent activity decreases and the muscle relaxes. Dynamic and

static responses of muscle spindle afferents influence

physio-

logical tremor

(see Clinical Box 9–2).

EFFECTS OF

γ

-MOTOR

NEURON DISCHARGE

Stimulation of

γ

-motor neurons produces a very different pic-

ture from that produced by stimulation of the extrafusal fibers.

Such stimulation does not lead directly to detectable contrac-

tion of the muscles because the intrafusal fibers are not strong

enough or plentiful enough to cause shortening. However,

stimulation does cause the contractile ends of the intrafusal fi-

bers to shorten and therefore stretches the nuclear bag portion

of the spindles, deforming the endings and initiating impulses

in the Ia fibers (Figure 9–4). This in turn can lead to reflex con-

traction of the muscle. Thus, muscle can be made to contract

via stimulation of the

α

-motor neurons that innervate the ex-

trafusal fibers or the

γ

-motor neurons that initiate contraction

indirectly via the stretch reflex.

If the whole muscle is stretched during stimulation of the

γ

• motor neurons, the rate of discharge in the Ia fibers is further
  increased (Figure 9–4). Increased
  γ
  -motor neuron activity
  thus increases
  spindle sensitivity
  during stretch.
  In response to descending excitatory input to spinal motor
  circuits, both
  α


• and
  γ
  -motor neurons are activated. Because
  of this “
  α


• 
  

  γ
  coactivation,” intrafusal and extrafusal fibers
  shorten together, and spindle afferent activity can occur
  throughout the period of muscle contraction. In this way, the
  spindle remains capable of responding to stretch and reflexly
  adjusting
  α
  -motor neuron discharge.

  
  

FIGURE 9–3
Diagram illustrating the pathways responsible
for the stretch reflex and the inverse stretch reflex.
Stretch stimu-
lates the muscle spindle, which activates Ia fibers that excite the motor
neuron. Stretch also stimulates the Golgi tendon organ, which acti-
vates Ib fibers that excite an interneuron that releases the inhibitory
mediator glycine. With strong stretch, the resulting hyperpolarization
of the motor neuron is so great that it stops discharging.

Motor endplate

on extrafusal fiber

Ventral root

Motor neuron

Dorsal root

Interneuron releasing

inhibitory mediator

Ib fiber

from

Golgi

tendon

organ

from

muscle

spindle

Ia fiber